ACYP1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout pool derived from the HT29 colorectal adenocarcinoma cell line. This product features targeted disruption of the ACYP1 gene via Cas9-mediated genome editing, resulting in a heterogeneous population of cells with diverse loss-of-function mutations. The polyclonal format avoids the biases of single-cell cloning while providing a robust genetic model for studying ACYP1 function in intestinal epithelial biology and cancer.
The HT29 cell line, isolated from a primary colorectal adenocarcinoma of a 44-year-old female, is an adherent epithelial model capable of enterocytic differentiation. It is widely employed in colorectal cancer studies and drug absorption assays due to its transformed phenotype and ease of genetic manipulation. This host cell background enables investigation of metabolic pathways in a context relevant to intestinal tumor biology and pharmaceutical development.
ACYP1 encodes an acylphosphatase that hydrolyzes acetyl phosphate and carbamoyl phosphate, key intermediates in glycolysis and pyruvate metabolism. Its expression is transcriptionally regulated by HIF1A and MYC and is responsive to metabolic stress. By modulating levels of these acylphosphates, ACYP1 directly influences glycolytic flux and cellular energy homeostasis. The enzyme functions within a metabolic network that includes pyruvate kinase and phosphoglycerate kinase, and its disruption can lead to accumulation of acetyl phosphate, which may serve as a phosphate donor or signaling molecule, thereby altering metabolic and proliferative states.
In HT29 colorectal cancer cells, ACYP1 knockout provides a model to study the impact of acylphosphatase loss on cancer metabolism. The accumulation of substrates like acetyl phosphate may shift glycolytic balance and affect pyruvate metabolism, potentially exposing metabolic vulnerabilities in tumor cells that rely on enhanced glycolysis. This system is particularly useful for exploring how colorectal cancer cells adapt to metabolic stress and for identifying pathways that can be targeted therapeutically.
This ACYP1 knockout polyclonal pool is ideal for colorectal cancer metabolism studies, metabolic drug target validation, and functional genomics screening. Representative assays include Seahorse metabolic flux analysis to measure glycolytic and mitochondrial respiration, Western blotting and RT-qPCR for ACYP1 expression analysis, and cell-based assays evaluating proliferation, apoptosis, migration, invasion, and colony formation. Drug sensitivity profiling can be performed to assess responses to metabolic inhibitors and chemotherapeutics. The heterogeneous polyclonal population provides a robust platform for studying ACYP1 loss-of-function effects in a colorectal adenocarcinoma context. For further information, please contact Ascent Research.
